Chronic exercise enhances cardiac alpha 1-adrenergic inotropic responsiveness in rats with mild hypertension

The singular and combined effects of mild renovascular hypertension (HTN) and chronic exercise on the contractile responsiveness of the heart to alpha 1-adrenergic receptor (alpha 1-AR) stimulation were determined. Age-matched normotensive and HTN male Fischer-344 rats were assigned to sedentary control or treadmill training groups. Left ventricular (LV) contractile performance was assessed by utilizing a modified isovolumic heart preparation at varying concentrations of phenylephrine (PE). Groups studied were normotensive sedentary (NSD), hypertensive sedentary (HSD), normotensive trained (NTR), and hypertensive trained (HTR). PE elicited increases in LV developed pressure (delta P), LV maximal rate of pressure development (dP/dt(max)), and LV dP/dt(max)/delta P in all experimental groups in a dose-dependent fashion. These PE-induced effects were representative of alpha 1-AR-mediated responses because they were observed in the presence of beta-adrenoceptor blockade with propranolol. Relative to NSD, the effects of PE on contractile function were attenuated in HSD and augmented in NTR and HTR hearts. The strength of extrasystolic contractions elicited by the delivery of a 300-ms extrasystolic interval at each of three different pacing frequencies (240, 270, and 300 beats/min) was greater in NTR and HTR and significantly reduced in HSD compared with NSD. Scatchard analysis of 3Hprazosin binding was used to assess alpha 1-AR number in myocardium isolated from each experimental group. Across all groups, a significant correlation was found between alpha 1-AR number and the inotropic responsiveness of the heart to PE stimulation. Collectively, these data provide evidence that mild HTN diminishes while training augments the inotropic responsiveness of the heart to alpha 1-AR stimulation. In addition, training appears to attenuate the adverse effects of mild HTN on the alpha 1-AR contractile responsiveness of the myocardium.